{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNR3C1, which encodes the glucocorticoid receptor (GR), plays a central role in regulating the hypothalamic–pituitary–adrenal (HPA) axis and mediating stress responses. Studies have shown that early‐life experiences—ranging from variations in maternal care to childhood maltreatment—can lead to epigenetic modifications at the NR3C1 promoter, thereby altering GR expression and influencing subsequent neuroendocrine function and risk for stress‐related psychopathology. These epigenetic changes, including differential cytosine methylation patterns, have been observed in both animal models and human postmortem brain and peripheral tissues, underscoring the importance of early environmental factors in programming lifelong HPA axis responsiveness."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "6"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, NR3C1/GR functions as a ligand-dependent transcription factor whose activity is finely regulated by multiple mechanisms. GR binds glucocorticoids with high affinity and, upon ligand binding, undergoes conformational changes that promote its translocation to the nucleus. There it interacts with specific glucocorticoid response elements (GREs) in DNA—which can themselves act as allosteric ligands—to tailer its conformation and regulatory output. In addition, GR activity is modulated by a spectrum of post-translational modifications, differential translational initiation generating multiple receptor isoforms, and interactions with molecular chaperones (e.g. Hsp90, Hsp70) and immunophilins (e.g. FKBP51 and FKBP52) that affect receptor stability, nuclear trafficking, and cofactor recruitment. These coordinated mechanisms ensure that GR regulates a unique set of target genes in a cell- and context-specific manner, thereby impacting processes such as metabolism, inflammation, and cell survival."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "7", "end_ref": "24"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic variations and polymorphisms within NR3C1 further influence glucocorticoid sensitivity and have been linked to a variety of clinical outcomes. Specific NR3C1 alleles and splice variants (including polymorphic sites such as N363S, ER22/23EK, and variations associated with the BclI region) can result in altered receptor function, ranging from hypersensitivity to resistance to glucocorticoids. These genotype-dependent differences contribute to individual variability in metabolic parameters, neuroendocrine feedback regulation, and vulnerability to stress-related disorders such as depression, posttraumatic stress disorder, and even certain forms of cancer and autoimmune conditions. Collectively, these findings highlight how both epigenetic programming and genetic diversity of NR3C1 underpin its critical regulatory functions in maintaining homeostasis and modulating disease risk."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "25", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Tim F Oberlander, Joanne Weinberg, Michael Papsdorf, et al. 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